【佳學(xué)基因檢測(cè)】基因檢測(cè)LINC00152了解肺腺癌轉(zhuǎn)移的治療靶點(diǎn)

全國十大基因檢測(cè)公司排名簡(jiǎn)介

研討《腫瘤致病基因突變位點(diǎn)的性質(zhì)及影響分析》《Cell Death Dis》在. 2022 Sep 7;13(9):772.發(fā)表了一篇題目為《TGF-β誘導(dǎo)的LINC00152通過HuR促進(jìn)肺腺癌轉(zhuǎn)移》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Wei Xu #, Linna Chen #, Jiheng Liu, Zhezhe Zhang, Ranran Wang, Qianqian Zhang, Huiting Li, Juanjuan Xiang, Li Fang, Ping Xu, Zheng Li 等完成。促進(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展，進(jìn)一步強(qiáng)調(diào)了基因信息檢測(cè)與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究?jī)?nèi)容關(guān)鍵詞：

基因檢測(cè),治療靶點(diǎn),肺腺癌,TGF-beta

腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果

肺腺癌（LUAD）是癌癥相關(guān)死亡的主要原因之一，具有早期轉(zhuǎn)移的強(qiáng)烈趨勢(shì)。轉(zhuǎn)化生長因子-β (TGF-β) 信號(hào)傳導(dǎo)是促進(jìn) LUAD 轉(zhuǎn)移的強(qiáng)大調(diào)節(jié)劑。在這里，肺腺癌轉(zhuǎn)移基因檢測(cè)及治療靶點(diǎn)尋找團(tuán)隊(duì)篩選了對(duì)TGF-β有反應(yīng)并在LUAD細(xì)胞中高表達(dá)的長鏈非編碼RNA（lncRNA），賊終獲得了肺腺癌轉(zhuǎn)移基因檢測(cè)研究中的主分子LINC00152。肺腺癌轉(zhuǎn)移基因檢測(cè)及治療靶點(diǎn)尋找團(tuán)隊(duì)證明 TGF-β 通過經(jīng)典的 TGF-β/SMAD3 信號(hào)通路促進(jìn) LINC00152 的轉(zhuǎn)錄，并通過 RNA 結(jié)合蛋白 HuR 保持其穩(wěn)定性。此外，LINC00152 通過增加 HuR 與這些轉(zhuǎn)錄因子的相互作用增加 ZEB1、SNAI1 和 SNAI2 的表達(dá)，賊終促進(jìn) LUAD 細(xì)胞的上皮間質(zhì)轉(zhuǎn)化并增強(qiáng) LUAD 在體內(nèi)的轉(zhuǎn)移。這些數(shù)據(jù)提供了證據(jù)表明由TGF-β誘導(dǎo)的LINC00152促進(jìn)肺腺癌中依賴于HuR的轉(zhuǎn)移。因此，設(shè)計(jì)靶向 LINC00152 和 HuR 抑制劑可能是 LUAD 治療的有效治療策略。

腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國際數(shù)據(jù)庫描述：

Lung adenocarcinoma (LUAD) is one of the main causes of cancer-related mortality, with a strong tendency to metastasize early. Transforming growth factor-β (TGF-β) signaling is a powerful regulator to promote metastasis of LUAD. Here, we screened long non-coding RNAs (lncRNAs) responsive to TGF-β and highly expressed in LUAD cells, and finally obtained our master molecular LINC00152. We proved that the TGF-β promoted transcription of LINC00152 through the classical TGF-β/SMAD3 signaling pathway and maintained its stability through the RNA-binding protein HuR. Moreover, LINC00152 increased ZEB1, SNAI1 and SNAI2 expression via increasing the interactions of HuR and these transcription factors, ultimately promoting epithelial-mesenchymal transition of LUAD cell and enhancing LUAD metastasis in vivo. These data provided evidence that LINC00152 induced by TGF-β promotes metastasis depending HuR in lung adenocarcinoma. Designing targeting LINC00152 and HuR inhibitors may therefore be an effective therapeutic strategy for LUAD treatment.